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Despite extensive research over the past few decades, the exact cause of rheumatoid arthritis (RA) has not yet been determined. In general, the following theories have been proposed in an attempt to explain what "triggers" the chronic inflammatory process that leads to the development of rheumatoid arthritis:

• Genetic predisposition
• Autoimmune disease
• Infections

Genetic Predisposition

This theory proposes that some people may be genetically predisposed to developing rheumatoid arthritis (RA). Support for this theory comes from studies in twins as well as in families which have found that the chances for developing RA is higher in individuals with a family history of the disease. A specific genetic "marker" , which is often found in a specific gene, the HLA-DR gene and especially in its HLA-DR4 subtype , tends to occur more frequently in people with RA than in the general population. This finding lends additional support for a genetic basis of the disease.

Autoimmune Disease

Proponents of this theory argue that rheumatoid arthritis (RA)is an autoimmune disease in which the body's own immune system turns against itself by attacking the joints. Support for this theory is based on the fact that most patients with RA produce an autoantibody (an abnormal antibody that attacks the body's own tissues) called rheumatoid factor (RF) that can be detected with a blood test. Rheumatoid factor is an autoantibody belonging to the IgM class of antibodies that binds to normal antibodies to produce an antigen-antibody complex. Formation of these antigen-antibody complexes in the joints is thought to serve as the "trigger" for initiating the chronic inflammatory response leading to the development of rheumatoid arthritis. A majority of patients with RA also have an antibody against cyclic citrulinated proteins (anti-CCP antibody). This antibody is highly specific for RA and is rarely found in people without RA or people with other diseases. Anti-CCP antibody may be detected before the onset of RA.

Infections

Some researchers have proposed that infections with microorganisms, such as bacteria and viruses, may be the primary precipitating event that causes rheumatoid arthritis (RA) in patients who are genetically predisposed to the disease. Support for this theory is based on the observation that recurrent infections often coincide with periods of "flare-ups" of rheumatoid arthritis.